This paper argues that the consensus physicalist antireductionism in the philosophy of biology cannot accommodate the research strategy or indeed the recent findings of molecular developmental biology. After describing Wolperts programmatic claims on its behalf, and recent work by Gehring and others to identify the molecular determinants of development, the paper attempts to identify the relationship between evolutionary and developmental biology by reconciling two apparently conflicting accounts of bio-function – Wrights and Nagels (as elaborated by Cummins). Finally, the paper seeks (...) a way of defending the two central theses of physicalist antireductionism in the light of the research program of molecular developmental biology, by sharply reducing their metaphysical force. (shrink)

This is a critical notice of Evolution's Eye by Susan Oyama, focusing on developmental systems theory primarily in relation to the nature-nurture debates and the explanation of behaviour.

The question of the influence of genes on behavior raises difficult philosophical and social issues. In this paper I delineate what I call the Developmentalist Challenge (DC) to assertions of genetic influence on behavior, and then examine the DC through an indepth analysis of the behavioral genetics of the nematode, C. elegans, with some briefer references to work on Drosophila. I argue that eight "rules" relating genes and behavior through environmentally-influenced and tangled neural nets capture the results of developmental and (...) behavioral studies on the nematode. Some elements of the DC are found to be sound and others are criticized. The essay concludes by examining the relations of this study to Kitcher's antireductionist arguments and Bechtel and Richardson's decomposition and localization heuristics. Some implications for human behavioral genetics are also briefly considered. (shrink)

I begin by examining how genetics drivesschizophrenia research, and raise both familiar andrelatively novel criticisms of the evidence putativelysupporting the genetic basis of schizophrenia. Inparticular, I call attention to a set of concernsabout the effects of placentation on concordance ratesof schizophrenia in monozygotic twins, which furtherweakens the case for schizophrenia''s so-called stronggenetic component. I then underscore two criticalpoints. First, I emphasize the importance of takingseriously considerations about the complexity of bothontogenesis and the development of hereditarydiseases. The recognition of developmentalconstraints and (...) supports is crucial, for attention todevelopment exposes the naivete of too many models ofgene action in the aetiology of disease. Secondly, Iattend to those schizophreniologists who ignoremethodological criticisms and thus presume a geneticbasis for schizophrenia, and then seek the schizophrenic genotype lacking an adequatephenotype. In response I attempt to demonstrate thenecessity of a sustained effort at characterizing thephenotype of schizophrenia as an enabling conditionfor the whole enterprise of psychiatric genetics – andfor psychiatry itself. Without the organism-levelphenotype, research at the level of genes will remainunproductive – assuming of course that research at thegenetic level is appropriate at all. (shrink)

Kenneth C. Schaffner's paper is an important contribution to the literature on behavioral genetics and on genetics in general. Schaffner has a long record of injecting real molecular biology into philosophical discussions of genetics. His treatments of the reduction of Mendelian to molecular genetics first drew philosophical attention to the problems of detail that have fuelled both anti-reductionism and more sophisticated models of theory reduction. An injection of molecular detail into discussions of genetics is particularly necessary at the present time, (...) when so many philosophers seem happy to discuss the philosophical and ethical implications of molecular biology using gene concepts derived from evolutionary biology ). Schaffner has long advocated the view that the philosophy of biology should be more than the philosophy of evolution. This paper shows how radically a picture of gene action derived from molecular biology undercuts the popular picture associated with a more evolutionary view of genes as units of heredity or as ‘difference-makers’ mediated by the ‘black box’ of development. (shrink)

Many recent gene knockout experiments cause anatomical changes to the jaw region of mice that several investigators claim are evolutionary reversals. Here we evaluate these mutant phenotypes and the assertions of atavism. We argue that following the knockout of Hoxa-2, Dlx-2, MHox, Otx2, and RAR genes, ectopic cartilages arise as secondary consequences of disruptions in normal processes of cell specification, migration, or differentiation. These disruptions cause an excess of mesenchyme to accumulate in a region through which skeletal progenitor cells usually (...) migrate, and at a site of condensation that is normally present in mammals but that is too small to chondrify. We find little evidence that these genes, when disrupted, cause a reversion to any primitive condition and although changes in their expression may have played a role in the evolution of the mammalian jaw, their function during morphogenesis is not sufficiently understood to confirm such hypotheses. BioEssays 20:245–255, 1998.© 1998 John Wiley & Sons, Inc. (shrink)